脑-肠互动在肠易激综合征发病中的作用

肠易激综合征(IBS)发病机制尚未完全阐明.目前研究认为,其发病机制与胃肠动力异常、内脏高敏感性、肠道感染、脑-肠互动、脑肠肽和受体以及社会心理因素有关,而脑-肠互动在IBS发病中的作用引起研究者的普遍关注,IBS上述的发病因素均可整合到脑-肠互动框架中进行阐述,脑-肠互动是研究IBS发病机制的切入点.本文从脑-肠轴及脑-肠互动,IBS发病因素与脑-肠互动以及临床治疗研究3个方面阐述脑-肠互动在IBS发病中的重要作用,以揭示脑-肠互动病理生理实质.     

脑-肠轴失调在肠易激综合征发病中作用的研究进展

肠易激综合征(IBS)的发生是多因素共同作用的结果,其发病机制尚未明确。近年来,以脑-肠轴为基础的生物-心理-社会医学模式参与IBS发病的观念被广泛接受。由神经-内分泌-免疫网络介导的脑-肠双向调节通路,在维持中枢神经系统与肠道局部稳态中发挥重要调节作用,其中任一环节异常,都可能导致稳态平衡破坏而诱发IBS。本文就脑-肠轴失调在IBS发生、发展中作用的研究进展作一综述。     

肠易激综合征发病机制的研究进展

肠易激综合征(IBS)的发病机制虽然仍不十分明确,但近年来除了在内脏高敏、肠动力异常等传统观点认为的病理生理基础上有新的发现外,在其他多方面均有重要的研究进展。此文从基因易感性、神经递质、感染及免疫、肠黏膜屏障、神经系统、精神心理因素、动物模型等方面较完整的对IBS发病机制的研究进展作一综述。     

肥大细胞异型性在肠易激综合征发病机制中的作用研究

目的　探讨肥大细胞在肠易激综合征 (IBS)患者肠道内分布、变化及其临床意义 ,并对其异型性在IBS发病机制中的作用进行相关研究。方法　经结肠镜钳取 2 4名正常人和 5 9例肠易激综合征患者回肠末端、盲肠和降结肠黏膜 ,分别采用抗人肥大细胞类胰酶抗体标识肥大细胞 ,并应用免疫组化方法检测了肥大细胞数目、活性变化和其雌激素受体表达的差异。结果　 1 IBS患者回肠末端和盲肠黏膜肥大细胞数目增多、活性增强 ,降结肠黏膜肥大细胞数目与正常组无显著差别 ,但腹泻型IBS患者降结肠肥大细胞活性增强 (P <0 .0 1)。 2 肥大细胞与雌激素受体阳性 (ER + )细胞显著相关 (R =0 .884,P <0 .0 1) ,但每例肥大细胞和ER +细胞的积分不同。结论　回肠末端和盲肠肥大细胞活性增强提示此处可能为IBS发病的关键部位 ;肥大细胞异型性与IBS病理生理过程密切相关     

肥大细胞及其雌激素受体在肠易激综合征发病机制中的作用

目的 探讨肠易激综合征(IBS)患者肠道内雌、孕激素受体阳性细胞和肥大细胞相关性及其临床意义。方法 经结肠镜钳取24名正常人和59例肠易激综合征患者回肠末端、盲肠和降结肠黏膜，分别采用抗人肥大细胞类胰酶抗体标识肥大细胞和抗人雌、孕激素受体抗体标识肠黏膜上雌、孕激素受体；同时应用免疫组化双染(DAB和BCIP／NBT染色)检测肥大细胞上雌激素受体的存在。结果 雌激素受体阳性细胞与肥大细胞显著相关，相关系数为0．884(P＜0．01)；肠道黏膜未见孕激素受体表达；IBS患者回肠末端和回盲部黏膜肥大细胞有雌激素受体表达。结论 肥大细胞为雌激素在消化道的重要靶点，肥大细胞上存在雌激素受体在IBS病理生理过程中发挥一定作用。     

结肠黏膜肥大细胞活化在肠易激综合征发病中的作用

目的　探讨结肠黏膜肥大细胞活化在肠易激综合征 (IBS)发病机制中的作用。方法　采用c Fos和类胰蛋白酶免疫组化双标方法 ,对应激和条件应激肠功能紊乱大鼠及符合罗马Ⅱ标准、连续就诊的发作期IBS患者 5 6例进行直肠乙状结肠交界处黏膜肥大细胞活化程度研究 ,并与对照大鼠和健康对照组及 2例无症状超过 6个月的IBS患者相比较 ,观察应激和条件应激大鼠在应激前 30min腹腔注射 (i.p .)肥大细胞稳定剂色甘酸二钠 2 0mg/kg对大鼠内脏敏感性的影响 ,通过Spearman等级相关分析评价IBS患者症状严重指数与肥大细胞活化分数的关系。结果　与对照组相比 ,应激 [(8.0± 0 .9)比(2 .5± 0 .8) ]和条件应激 [(7.8± 0 .8)比 (2 .5± 0 .8) ]大鼠结肠下段黏膜活化细胞明显增加 ,但肥大细胞总数无明显改变 ;色甘酸二钠显著降低应激大鼠 [(7.2± 1.2 )比 (3.8± 0 .8) ,P <0 .0 1]和条件应激大鼠[(6 .8± 0 .8)比 (3.8± 0 .8) ,P <0 .0 1]的内脏敏感性 ,对对照组大鼠却无影响。与 2 0例正常对照组相比 ,IBS发作期患者直肠乙状结肠交界处黏膜肥大细胞数目和活化细胞分数显著增加 [(85± 12 )比 (15± 6 ) ,P <0 .0 1],肥大细胞活化分数与症状严重程度指数显著相关 (r =0 .86 2 ,P <0 .0 1)。结论　肠道黏膜肥大细胞活化     

肠易激综合征的发病机制

肠易激综合征 (ｉｒｒｉｔａｂｌｅｂｏｗｅｌｓｙｎｄｒｏｍｅ ,ＩＢＳ)是一种常见的以腹痛 /腹部不适伴排便习惯改变为特征的功能性肠病 (ｆｕｎｃｔｉｏｎａｌｂｏｗｅｌｄｉｓｅａｓｅ ,ＦＢＤ) ,缺乏形态学和生化学改变的生物学标志。该病发病率高 ,美国人群患病率约为 2 0 % ,北京市人群患病率按Ｍａｎｎｉｎｇ标准和罗马标准分别为 7.2 6%和 0 .82 %。曾被称为粘液性肠炎、结肠痉挛、结肠过敏、过敏性结肠炎、易激结肠等易混淆的术语 ,现统一命名为肠易激综合征[1] 。其病因和发病机制复杂 ,迄今尚不完全清楚 ,一般认为ＩＢＳ是个体…     

脑诱发电位与功能性脑成像在肠易激综合征研究中的应用

肠易激综合征(Irritablebowelsyndmme，IBS)是腹部不适或腹痛伴排便异常的一组肠功能障碍综合征，因其缺乏明显形态学及生化异常，病因及发病机制不甚清楚，给诊断及治疗带来了许多困难。近年来，IBS患者内脏感觉异常这一病理生理改变受到广泛关注，为深入了解内脏感觉异常的神经生物学机制，最近几种可客观评价IBS患者感觉传入通路及大脑信息处理过     

从肠易激综合征脑肠轴学说谈肝郁脾虚病理机制

运用肠易激综合征（IBS）脑肠轴学说,探讨中医学对IBS肝郁脾虚病理机制的认识有望是现今该领域的一个突破点.借用功能磁共振成像（fMRI）等技术,已发现IBS患者与疼痛和情感处理有关的脑区域内活动激活状态与健康人明显不同,提示其中枢神经系统对外周疼痛传入的下调功能减弱.     

肠康方对肠易激综合征内脏高敏感模型大鼠脑肠轴中5-羟色胺转运体的作用

目的:探讨肠康方对肠易激综合征(irritable bowel syndrome,IBS)内脏高敏感模型大鼠脑-肠轴中5-羟色胺转运体(serotonin transporter,SERT)的作用.方法:将72只SD幼♂大鼠随机分为空白对照组和造模组.采用AL-Chaer方法造模,将成功造模后的大鼠随机分为模型组、阳性药物对照组、肠康方高剂量组、中剂量组及低剂量组.第70天取脑、肠组织制作标本,应用免疫组织化学技术检测SERT的表达.结果:IBS内脏高敏感模型大鼠具有肠黏膜与脑组织SERT的低表达(0.16±0.05,P<0.05;0.10±0.04,P<0.001);肠康方高剂量治疗后肠黏膜(0.41±0.11,P<0.001)与脑组织(0.19±0.05,P<0.001)中SERT表达水平显著增高;肠康方中剂量治疗后肠黏膜(0.36±0.10,P<0.001)与脑组织(0.14±0.03,P<0.05)SERT表达水平也显著增高.结论:肠康方可调控IBS内脏高敏感模型大鼠脑-肠轴中SERT表达来治疗IBS.     

Neuroimaging the brain-gut axis in patients with irritable bowel syndrome

AIM:To summarize and synthesize current literature on neuroimaging the brain-gut axis in patients with irritable bowel syndrome(IBS).METHODS:A database search for relevant literature was conducted using Pub Med,Scopus and Embase in February 2015.Date filters were applied from the year2009 and onward,and studies were limited to those written in the English language and those performed upon human subjects.The initial search yielded 797articles,out of which 38 were pulled for full text review and 27 were included for study analysis.Investigations were reviewed to determine study design,methodology and results,and data points were placed in tabular format to facilitate analysis of study findings across disparate investigations.RESULTS:Analysis of study data resulted in the abstraction of four key themes:Neurohormonal differences,anatomic measurements of brain structure and connectivity,differences in functional responsiveness of the brain during rectal distention,and confounding/correlating patient factors.Studies in this review noted alterations of glutamate in the left hippocampus(HIPP),commonalities across IBS subjects in terms of brain oscillation patterns,cortical thickness/gray matter volume differences,and neuroanatomical regions withincreased activation in patients with IBS:Anterio cingulate cortex,mid cingulate cortex,amygdala anterior insula,posterior insula and prefrontal cortex.A striking finding among interventions was the substantia influence that patient variables(e.g.,sex,psychologica and disease related factors)had upon the identification of neuroanatomical differences in structure and con nectivity.CONCLUSION:The field of neuroimaging can provide insight into underlying physiological differences that distinguish patients with IBS from a healthy population.     

Sleep and gastric function in irritable bowel syndrome: derailing the brain-gut axis

Background—Recently, several studies have shown analteration in bowel function during sleep in patients with irritablebowel syndrome (IBS), and a recent study also suggests a remarkable increase in rapid eye movement (REM) sleep. These studies have suggested that an alteration in CNS function may play an important rolein the pathogenesis of IBS.
Aims—To confirm the presence of an alteration inREM sleep in patients with IBS and to assess the relation between sleepand a non-invasive measure of gastric functioning, theelectrogastrogram (EGG).
Patients—Ten patients with IBSand 10 age and sexmatched normal volunteers.
Methods—All subjects slept one night in the sleeplaboratory and underwent polysomnographic monitoring to determinesleep patterns, and recording of the EGG from surface electrodes.
Results—The IBS group had a notable andsignificant increase in the percentage and duration of REM sleep(p<0.05). The control group had a decrease in the amplitude of thedominant EGG frequency from waking to non-REM sleep (p<0.05), and asubsequent increase in the amplitude from non-REM to REM sleep(p<0.05). No such changes were noted in the patients with IBS.
Conclusions—Results confirmed the enhancement ofREM sleep in patients with IBS and suggested an intrinsic alteration inautonomic and CNS functioning in patients with IBS.

Keywords:sleep; irritable bowel syndrome; gastric function; brain/gut

     

从脑-肠互动的高度认识肠易激综合征

肠易激综合征 (IBS)的病因和发病机制目前尚未完全清楚。大量研究证明 ,胃肠动力与内脏感觉异常是IBS病理生理学的主要特征。亦已证明 ,IBS患者的精神心理异常 ,高于一般人。近年研究还发现 ,急性胃肠感染后IBS发病率显著增高。上述改变反映了IBS发病的不同侧面。近年来随着神经胃肠病学研究的发展 ,有越来越多的研究试图从脑 肠互动的高度 ,把上述不同因素整合起来 ,从更深的层次去揭示IBS的病因和发病机制[1] 。胃肠道有一个从一级感觉神经元、中间神经元到支配胃肠效应的运动神经元组成的、独立于大脑之外的神经系统 ,被称为肠…     

肠易激综合征发病机制研究进展

肠易激综合征(irritable bowel syndrome, IBS)是常见的功能性胃肠病, 其发病机制尚未完全阐明.目前认为IBS是由多种因素共同作用的结果, 肠道动力异常, 内脏高敏感性为IBS发病的病理生理基础.本文对IBS的多种发病机制的最新研究作一综述.     

Gene, environment, and brain-gut interactions in irritable bowel syndrome

The genetic predisposition and influence of environment may underlie in the pathogenesis and/or pathophysiology of irritable bowel syndrome (IBS). This phenomenon, gene x environment interaction together with brain-gut interactions is emerging area to be clarified in IBS research. Earlier studies focused on candidate genes of neurotransmitters, cytokines, and growth factors. Among them, some studies but not all studies revealed association between phenotypes of IBS and 5-hydroxytryptamine (5-HT)-related genes, noradrenaline-related genes, and cytokine genes. Recent prospective cohort study showed that genes encoding immune and adhesion molecules were associated with post-infectious etiology of IBS. Psychosocial stressors and intraluminal factors especially microbiota are keys to develop IBS. IBS patients may have abnormal gut microbiota as well as increased organic acids. IBS is disorder that relates to brain-gut interactions, emotional dysregulation, and illness behaviors. Brain imaging with or without combination of visceral stimulation enables us to depict the detailed information of brain-gut interactions. In IBS patients, thalamus, insula, anterior cingulate cortex, amygdala, and brainstem were more activated in response to visceral stimulation than controls. Corticotropin-releasing hormone and 5-HT are the candidate substances which regulate exaggerated brain-gut response. In conclusion, gene x environment interaction together with brain-gut interactions may play crucial roles in IBS development. Further fundamental research on this issue is warranted.     

肠易激综合征发病机制的研究进展

肠易激综合征(irritable bowel syndrome,IBS)是一种以腹部不适和排便习惯改变为特征的胃肠功能性疾病.IBS的发病机制仍不清楚,传统观点认为基因、心理社会因素、胃肠动力障碍和内脏高敏感性等是引起IBS的关键因素.近年来,人们陆续发现了一些与IBS发病相关的新病理生理学改变依据,如脑肠轴调节失常、肠道感染、肥大细胞的激活并释放活性物质等.本文总结与IBS发病机制相关的一些最新研究进展.     

肠易激综合征发病机制研究进展

肠易激综合征（irritable bowel syndrome,IBS）是常见的功能性肠病,以腹痛伴有大便性状和排便习惯改变为主 要表现。IBS 发病机制复杂,包括了增加IBS易感性的因素及与症状发作相关的因素,多种因素相互作用导致了相应 的病理生理变化,从而产生IBS症状,文章就已有的研究结果对IBS的发病机制进行总结。     

Genetic polymorphism in pathogenesis of irritable bowel syndrome

Irritable bowel syndrome(IBS)is a complex symptombased disorder without established biomarkers or putative pathophysiology.IBS is a common functional gastrointestinal disorder which is defined as recurrent abdominal pain or discomfort that has at least two of the following symptoms for 3 d per month in the past 3mo according to ROMEⅢ:relief by defecation,onset associated with a change in stool frequency or onset with change in appearance or form of stool.Recent discoveries revealed genetic polymorphisms in specific cytokines and neuropeptides may possibly influence the frequencies and severity of symptoms,as well as the therapeutic responses in treating IBS patients.This review gives new insights on how genetic determinations influence in clinical manifestations,treatment responses and potential biomarkers of IBS.